The hypothesis proposed suggests that the anorexia, in association with neoplastic disease, is secondary to peripheral metabolic changes which are induced by the presence of the tumor. This deranged metabolism in turn, results in derangements in lipid and carbohydrate metabolism, resulting in an excess of plasma non-esterified fatty acids. The penetration of tryptophan through the blood-brain barrier depends on a host of factors including the ratios between tryptophan and other competing neutral amino acids, the amount of free or unbound tryptophan, as well as the amount of tryptophan bound to albumin. In neoplastic disease, there is an increase in non-esterified fatty acids which displace tryptophan from albumin, making it more available for entry across the blood-brain barrier. Investigations to date have shown increased metabolism of brain tryptophan in two models of neoplastic disease, including a Walker 256 carcinosarcoma model and a MCA implantable tumor in adult rats. Other aspects include the use of blocking agents of serotonin metabolism to prevent or delay anorexia, as well as intraventricular installation of various materials. The results to date confirm the involvement of a distorted central tryptophan serotonin system in the anorexia of cancer.